Infections in burn patients: a paradigm for cutaneous infection in the patient at risk

The burn patient is in many ways the archetypical immunosuppressed host: the anatomic barriers have been breached and the host's defenses suppressed. Infection is the leading cause of death in hospitalized burn patients not having inhalation injury, being responsible for between 50 and 75 percent of the hospital deaths. Burn injury produces profound abnormalities in immunologic function. These changes are generally proportional to the degree of burn injury (surface area and depth). Cell-mediated immune function is suppressed. Anergy and depressed allograft rejection occur. Acute burn serum samples contain several factors that suppress cell-mediated immune functions. Antibody levels are usually mildly to moderately reduced. Complement, particularly the alternative complement pathway, may be massively activated and depleted, removing a critical defense mechanism against gram-negative rod infections for which preformed antibodies are absent. This depression is further exacerbated by malnutrition and infection. Fibronectin levels are also reduced. Phagocytic cell function is abnormal with burns. Neutrophil numbers may be depressed, and function is abnormal. Chemotactic responsiveness, cytoplasmic granule enzyme content, and oxygen radical generation are abnormal. Monocyte/macrophage dysfunction has similarly been demonstrated. Burn infections reflect abnormal host functions as well as changes in the hospital environment and microbial selection pressures. The burn patient is a model of cutaneous infection in the patient at risk.